2011 CCSVI Symposiums Videos Now Being Uploaded

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Squeakycat » Tue Sep 13, 2011 9:37 am

There are a total of 46 videos. So far, only the first two have been uploaded: Dr. Sclafani's Welcome and a fascinating presentation by Clive Beggs, PhD on Venous Hemodynamics in CCSVi and MS in which he shows that mechanically, blockages cause pressure to rise and profusion of blood to slow.

CCSVI Symposium 2011 - Second Annual Meeting
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby MrSuccess » Tue Sep 13, 2011 8:38 pm

I would like to see a separate thread started with discussions about
the fluid dynamics , only.
I found Clive Beggs video , most interesting .

Fluid is .........really and truly "dumb".

I am certain Trevor Tucker would welcome the challenge and contribute .


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For the record ..... most fluids CAN be compressed.
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Tue Sep 13, 2011 9:25 pm

excellent Squeakcat thanks for posting!
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Squeakycat » Tue Sep 13, 2011 11:52 pm

MrSuccess wrote:I would like to see a separate thread started with discussions about
the fluid dynamics , only.

I found Clive Beggs video , most interesting .

I am certain Trevor Tucker would welcome the challenge and contribute .


Great idea! Beggs might want to participate also. I'll look into that and start get the thread started.
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby cheerleader » Thu Sep 15, 2011 8:23 am

thanks, squeaky!
These are great videos.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby ttucker3 » Thu Sep 15, 2011 9:04 am

Happy to help if I can. However, I would like to see the involvement of one or two Fluid Dynamicists who also have an interest in cardiovascular flow. Fluid Dynamics is governed by the Navier-Stokes equations. These are the same equations that meteorologists use to predict the weather. They can see a bit into the future, but as one goes farther out the solutions get a bit chaotic (consistent with turbulent blood flow in veins).
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Fri Oct 14, 2011 6:58 pm

ttucker3 wrote:Happy to help if I can. However, I would like to see the involvement of one or two Fluid Dynamicists who also have an interest in cardiovascular flow. Fluid Dynamics is governed by the Navier-Stokes equations. These are the same equations that meteorologists use to predict the weather. They can see a bit into the future, but as one goes farther out the solutions get a bit chaotic (consistent with turbulent blood flow in veins).
Trev. Tucker

Really interesting. Even if I don't yet understand this. Does this mean that the effects of turbulent blood flow can best be predicted close to the blockage and are more chaotic/unpredictable further from the blockage, such as in the deep cerebral veins?
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Fri Oct 14, 2011 7:28 pm

Let's talk about Dr. Sclafani's opening remarks.

http://www.facebook.com/pages/CCSVI-in- ... 9784512383

I took notes while I watched this, they are at times verbatim but not completely so:
fortuitous that Zamboni had personal reasons and the right background as a vascular surgeon with expertise in veins/vein disease

Abnormalities in outflow of brain leads to exuberant retrograde flow through collateral vessels, some of which end up in the deep cerebral veins and result in a flow overload of small veins and that, he postulates, leads to loosening of tight junctions and diapedesis of red blood cells across the blood-brain barrier leading to hemosiderin deposits, iron deposition and inflammation of the brain. The theory puts the demyelination on the back end rather than the front end. And the autoimmunity as a response to dead tissue instead of the primary process.

Here the theory is all dressed up in accurate scientific words but it is the same theory that we know well. Our blocked veins are outflow obstructions. This leads to reflux. Some of the reflux goes all the way up to the deep cerebral veins. Shear stress and one-way flow strengthens veins; reflux and turbulent flow weakens them. The blood brain barrier has junctions ten times as tight as the capillaries anywhere else in the body. Reflux causes these junctions to loosen. Diapedesis is a beautiful word for the ugly leakage of red blood cells through that loosened blood brain barrier. This leads to hemosiderin iron deposits and inflammation.

One thing leads to the next thing leads to the next thing. It is simple and straight-forward, even if it seems complex.

Demyelination ends up on the back end, not the front end, meaning that it is secondary and not primary. Instead of an autoimmune disease causing demyelination, with an errant immune system being the cause, the immune system is acting appropriately in response to the dead tissue caused by the cascade of effects that are the result of the brain's outflow obstructions. This inflammation causes its own damage as well.

Dr. Sclafani's personal point-of-view: I don't think it's important. I think Dr. Zamboni made a mistake to make this association so strongly between the etiology of MS and the outflow obstructions of the brain. The outflow obstructions of the brain are, for anyone who has managed this process for any length of time, is clear-cut and overwhelming evidence. The veins are abnormal. And it's my postulate, and not Zamboni's, that some of the symptoms that we see in patients of MS are really the symptoms of outflow obstructions of the brain and not MS itself. That is one of the things we will try to determine in time. The rage has been in objection to the concept that venous obstructions can cause MS. But to the patients the rage has been that relieving obstructions to the brain improves their quality of life. So we have to reconcile that.

He's alluded to some of this before, but this is well explained. Would we have been better off if Dr. Zamboni had discovered just CCSVI, and not CCSVI in MS? I am not sure. The only reason I knew to go get my jugulars looked at was because of my MS diagnosis. MS and CCSVI are associated. But if we could look at just CCSVI, it becomes simpler.

I absolutely agree that some of the symptoms that were attributed to my MS have turned out to be CCSVI symptoms. Anything that disappeared on the table was a CCSVI symptom.

The question of whether or not CCSVI causes MS is academic. The question of whether relieving CCSVI obstructions can improve quality-of-life is deeply pressing. And for me, it has improved.
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby ttucker3 » Sun Oct 16, 2011 12:47 pm

Cece in response to your question of October 14:

"Really interesting. Even if I don't yet understand this. Does this mean that the effects of turbulent blood flow can best be predicted close to the blockage and are more chaotic/unpredictable further from the blockage, such as in the deep cerebral veins?"

What I was trying to convey with probably too few words was that measured venous blood flow in MS patients can be very complicated - with flow including: 1. sometimes going positive and then negative (toward heart then away from the heart) within a single time interval between pulses; 2. at some places in the vein having very little velocity over multiple pulse cycles , but at other points fairly substantial velocities existing, all simultaneously; 3. sometimes smooth and as expected; 4. sometimes being turbulent, going in both directions simultaneously at the same moment and spot in the vein. Solving the the fluid dynamics equations, the Navier-Stokes (NS) equations, using correct boundary conditions, particularly the compliance of the vein and surrounding tissues, the existence of webs, septums, etc, within the vein, the NS solutions that could be developed could include all of the above types of flow. I predict that within two to three years decent venous flow computation fluid dynamics software models will exist that produce good matches of predicted venous flow distribution to measurements (as hopefully obtained using a whole range of measurement techniques, including IVUS, flow quanitification and catheter MRV). I would predict it quite likely that not only could the impact of things like position and percentage obstruction be modeled on the flow distribution, but also other effects such as the difference in vein compliance between males and females, the effect of cigarette smoking and vitamin D on vein compliance and hypoxia's influence on endothelium (vein wall) strength, endothelial cell death, expression of endothelial-leukocye adhesion molecules, perhaps even hypoxia's triggering of angiogensis (growth of collaterals) by the endothelium. I hold out some hope that Computational Fluid Dynamics will one day permit the integration of all the major influences, not just flow obstructions, but also the influence of some of those other environmental, gender and genetic factors. This would provide substantial insight into the way in which these various influences interact in the development of MS.

What I was trying to say about the solutions becoming less and less accurate, I really meant less predictable as you try to look farther into the future. As time goes by the solutions of such equations change and become less predictable, just as the weather changes as time goes by. Indeed, the Navier-Stokes are the same equations that meteorologists currently use to predict the weather. Historically, it was a meteorologist named Lorenzo, who, while using the Navier-Stokes equations identified what is now call "Chaotic Behaviour" (and there are many books available today that describe this behaviour). One of the chaotic properties is turbulent flow.

I know, as Belafonte once said, "it's as clear as mud, but it covers the ground"

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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Sun Oct 16, 2011 2:19 pm

I like those predictions. It is just something to imagine having answers, when it comes to MS and now CCSVI. I am used to this disease having unknowns.
What I was trying to convey with probably too few words

I think my lack of any physics background is the issue. I will work on this....
was that measured venous blood flow in MS patients can be very complicated - with flow including: 1. sometimes going positive and then negative (toward heart then away from the heart) within a single time interval between pulses;

This sounds like basic reflux, which I've seen measured on the Haacke protocol MRV
2. at some places in the vein having very little velocity over multiple pulse cycles ,

My own left jugular exhibited this, when the contrast just sat in the jugular, in stasis.
but at other points fairly substantial velocities existing, all simultaneously;

I don't understand the simultaneous part of this. I think of flow as going one way or another, not both at once.
So much to consider.
3. sometimes smooth and as expected;
4. sometimes being turbulent, going in both directions simultaneously at the same moment and spot in the vein.
Solving the the fluid dynamics equations, the Navier-Stokes (NS) equations, using correct boundary conditions, particularly the compliance of the vein and surrounding tissues, the existence of webs, septums, etc, within the vein, the NS solutions that could be developed could include all of the above types of flow.

It's a very interesting direction of inquiry. And it does not have to be all clear to me, as long as it is clear to you and to others working in CCSVI.
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Wed Nov 09, 2011 7:24 pm

notes from the panel on blood flow and CCSVI with Dr. Haacke, Dr. Zivadinov and Dr. Beggs

Dr. Haacke wonders if the people who do not benefit from CCSVI may have had normal flow to begin with. This correlation has not been looked at yet. Very important to compare MR to ultrasound data.

Dr. Sclafani: we have to explain why a significant number of patients have no clinical improvement after treatment of stenoses and perhaps this is the correlation we need to do for predictability.

[CECE'S COMMENTS: I AM NOT SURE IF THIS IS THE ANSWER (PEOPLE WHO DO NOT BENEFIT FROM CCSVI MAY NOT HAVE HAD ABNORMAL FLOW, ONLY ABNORMAL STENOSES) BUT I DO THINK THAT AS PATIENTS WE WOULD BENEFIT FROM PREDICTABILITY. GOING INTO THE PROCEDURE, WE DON’T KNOW WHO WILL BENEFIT AND WHO WON'T, AND IT'S VERY EXCITING TO BE IN THE GROUP THAT BENEFITS, BUT TERRIBLE TO BE IN THE GROUP THAT DOESN’T. IT WOULD ALSO HELP WITH THE CHOICE OF WHETHER TO PURSUE TREATMENT OR NOT, IF THERE WAS A GOOD WAY TO PREDICT IF YOU WOULD BE A RESPONDER. THE BENEFITS I'VE HAD WOULD HAVE BEEN WORTH $10,000. EASY. BUT THIS IS NOT TRUE FOR EVERYONE. OK, BACK TO THE SHOW.]

[DR. ZIVADINOV AND DR. BEGGS HAVE GREAT ACCENTS. VERY NICE TO LISTEN TO.]

Dr. Zivadinov shares some of his data. They implemented the flow data with the MRV in the last 150 patients as well as ultrasound data as well in the same individuals. It will be interesting to look at the correlation between CCSVI protocol parameters (flow, velocity studies.) the only paper until now is the Doepp study that looked at that and I don't think he appropriately assessed the CCSVI parameters. but probably very good flow and velocity studies. We look at the relationship between the amount of severity parameters of CCSVI venous insufficiency severity score created by Dr. Zamboni in respect to lesion volume. No relationship. We tried to diversify the damage in the left and right hemisphere and correlate it with the left and right jugular stenosis. No correlation.

[CECE'S NOTES: PHLEBOLOGIST HAS POSTED AT TIMS AN EXPLANATION FOR THIS LACK OF SIDED-NESS, SUCH AS A STENOSIS IN THE LEFT JUGULAR NOT LEADING TO LESIONS ON THE LEFT SIDE OF THE BRAIN. PHLEBOLOGIST SAID THAT THE FLOW FROM THE BRAIN POOLS IN THE SINUSES, SO ANY OUTFLOW OBSTRUCTION REGARDLESS OF SIDE AFFECTS THE ENTIRE BRAIN BECAUSE OF THAT POOLING. I HOPE I AM EXPLAINING THAT CORRECTLY.]

Maybe if we had enough early patients we would be able to find some correlation respective to the amount of stenosis.

[I MIGHT BE CONSIDERED AN EARLY PATIENT. ONLY ONE LESION. I HAD SEVERE STENOSES. BUT I HAD GREAT VERTS THAT COMPENSATED, TO SOME EXTENT, FOR MY SEVERE JUGULAR STENOSES. THERE IS ALSO VARIABILITY IN PEOPLE'S DEGREE OF IMMUNE REACTION TO THE DAMAGE OF CCSVI. THERE IS THE HEALTH OF THE ENDOTHELIUM. I THINK HE IS TALKING ABOUT VHISS SCORES?? DID WE EVER SEE DATA FROM ZAMBONI'S TEAM CORRELATING THE VHISS SCORE WITH WORSE DISABILITY OR WORSE MS?]

Dr. Haacke comments on variables. Age, length of duration of MS. With all these variables that can be classified as CCSVI, and there are dozens and dozens of variables, the only way to really address the questions is by doing thousands of cases. We wont' be able to address the age issue unless you have at least 20 per bin per age, and unless you can break those up into the parameters such as left and right jugular problems or vertebral problems, so we need to work together with a lot of groups to create a database that lets us assess all that. We don't want to wait 20 years to do this. The group here has already demonstrated very strong collaboration. I think it's critical to get such a working group together so the data can be shared. [COLLABORATION! BIG CHEERS.]

Dr. Beggs pulls the discussion back to the original question, of why some patients improve and some don't, and his suggestion is interesting. Purely theoretical. Fluids are dumb. They flow where the least resistance. What if there is resistance in the extracranial vessels (jugulars) but there is also some resistance in the capillary beds due to morphological change. Then you can do something about the extracranial stenoses in the jugulars with the endovascular intervention but you're not doing anything about the capillary beds or increased resistance there. So a good place to look in patients who do not improve, he would suggest they have an increased resistance in these other vessels. Pure hypothesis.

[OK THAT COULD BE WHAT'S HAPPENING BUT WHAT DO WE DO ABOUT IT?? IF THERE WAS INCREASED RESISTANCE IN THE CAPILLARY BEDS, COULD THIS BE MEASURED? WOULD TOTAL OUTFLOW BE AFFECTED AND MEASUREABLE? DID THE MORPHOLOGICAL CHANGE IN THE CAPILLARY BED HAPPEN AS A RESULT OF THE CCSVI? CAN IT BE UNDONE? I HAVE MORE STUDYING TO DO ON CEREBRAL CAPILLARIES….]

Dr. Beggs: you have to look at the whole circuit when you're dealing with flow if it's a sealed circuit, it can have lots of branches, but what comes out is what went in, so if you occlude that in any place, it affects the whole system. If resistance is increased, flow is reduced. Simple as that.

[SIMPLE AS THAT. I AM LIKING DR. BEGGS, HE BRINGS A NEW KNOWLEDGE BASE TO THE PROBLEM.]

Question from the audience: Can reflux be primary or is it always combined with stenosis?

Dr. Sclafani: I think we have to differentiate two types of reflux. One is reflux above an obstruction and reflux without an obstruction. If a valve is incompetent, there can be reflux but without an obstruction that is relatively simply dissipated. But with an obstruction, the reflux can extend into the deep veins.

Dr. Zivadinov: we are learning a lot through all these studies through the last two years about this problem. I did a doppler on myself and I have an abnormal valve. [!] That's why it's so important why we do healthy people and understand what problems they have. We measure the collateral veins in two studies using huge numbers of patients an healthy controls and 95% of healthy people have a big collateral vein in their neck. So to have a collateral vein in the neck, it is something physiological. If you have reflux, how important is that reflux? Is that a reason to go and be treated or is it something that all of us have? I think that flow velocity studies through MRI or ultrasound post and pre treatment are going to play a huge role if they are reliable and reproducible in determining who to treat, what to treat and is it necessary to treat. What if you reopen something and create a worse situation, for someone who had a dominant collateral that was draining the brain properly. We need to learn a lot in respect to flow dynamics of the brain and extracranials.

[WHAT DOES EVERYONE THINK ABOUT THAT? IS IT POSSIBLE TO REOPEN A JUGULAR AND CREATE A ROUTE THAT IS WORSE THAN THE COLLATERAL WAS? I THOUGHT BLOOD WAS DUMB, IT WOULD TAKE WHATEVER ROUTE THAT WAS BETTER, AND IF THAT WAS THE COLLATERAL, THAT WOULD STILL BE THERE FOR THE TAKING.]

Dr. Beggs: I think it's important to distinguish between reflux that lasts longer than the cardiac cycle and reflux that lasts periodically as part of the cardiac cycle. If it lasts longer than the cardiac cycle than it's not directly related to the pulsatile nature of the hemodynamic system of the brain but it 's some extracranial effect that's causing the circulation of the blood that's flowing by another route and it's drawing blood back so you're getting a circuitry effect. If it's in the cardiac cycle as Mark showed, I think the role of the cerebrospinal fluid is absolutely crucial to this, because it's almost like a harmonic circuit almost like a weight like a pendulum the cerebrospinal column has got inertia. The thing that tells me if you have something going up and down and it starts to pull a bit more then that starts to suck and that's where you'll start to see the reflux occurring. Look at the whole circuit and the timing. I'm not looking at it in the context of MS patients but I'm looking at it in terms of normal physiology because the normal physiology is not understood. There are a lot of wrong ideas out there. We have to understand that before we can then apply it to pathologies.

[I AM GLAD I WAS TYPING OUT WHAT DR. BEGGS WAS SAYING BECAUSE IT WAS RATHER FAST AND HIS IDEAS ARE NEW TO ME. I AGREE ABOUT THE PAUCITY OF RESEARCH ON WHAT IS NORMAL. I DO NOT FOLLOW WHAT HE WAS SAYING ABOUT A HARMONIC CIRCUIT OR THE INERTIA OF THE CEREBROSPINAL COLUMN. IF IT PULLS ON THE BOTTOM IT CREATES SUCTION AT THE TOP? WHY IS IT PULLING ON THE BOTTOM? LIKE A WEIGHT LIKE A PENDULUM. ANYONE WANT TO TRY EXPLAINING THIS? I MIGHT GET IT WHEN I GET TO HIS PRESENTATIONS.]

Dr. Haacke discussed jugular flow when sitting up. Doepp's research involved some of this. MS patients have some faulty relationship that doesn't let the vertebrals take over when they sit up. Esaote in Italy is looking at building an MRI system that would rotate from being vertical to horizontal.

[DR HAACKE LIGHTS UP A BIT WHEN TALKING ABOUT THE ROTATING MRI SYSTEM. BOYS AND THEIR TOYS…. BUT IT WOULD BE A USEFUL RESEARCH TOOL.]

Break time! Whew.
Last edited by Cece on Thu Nov 10, 2011 11:23 am, edited 1 time in total.
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Re: 2011 CCSVI Symposiums Videos Now Being Uploaded

Postby Cece » Wed Nov 09, 2011 8:45 pm

Integrating CCSVI into a busy ambulatory practice

[SO THAT'S DR SULLIVAN! I HADN'T SEEN HIM BEFORE.]

Credentialing is probably already in place

[CREDENTIALING IS THE PROCESS OF GETTING INSURANCE TO RECOGNISE YOU AS A PROVIDER WHO THEY WILL PAY.]

Affiliations: many capable, well-respected interventionalists have been prevented from performing CCSVI procedures because of their hospital affiliation.

[DR. DAKE. DR. MCDONALD. WHO WAS THE DOCTOR WHO HAD A PATIENT PREPPED TO GO, WHO WAS TOLD RIGHT THEN THAT HE COULD NOT DO ANY MORE? THIS WAS ALL LATE 2009 AND THEN EARLY-MID 2010. I THINK WE ARE PAST ALL THAT NOW….]

Free-standing center will still have some issues. Neurologists will be opposed. Patients will come to you with very different views. They are convinced this works and do not want to wait for trials which could take years. Messages online can get personal and negative. If you get involved in this and treat these patients, you may be the target of this as well.

[A GOOD REASON FOR ALL OF US ONLINE TO TAKE A LOOK AT OUR OWN WORDS AND MAKE SURE WE HAVE BEEN RESPECTFUL.]

Dr. Sullivan advises that the IR take a balanced perspective during the informed consent. Take time to answer questions in detail about what is known and not known. Don't promise more than can be delivered.

[OMG. DO YOU REMEMBER BLUESKY ASKING A CLINIC, EARLY ON, IF THEY HAD HANDICAPPED ACCESSIBILITY OR GUEST WHEELCHAIRS, I CAN'T REMEMBER WHAT EXACTLY, AND SHE WAS TOLD IT DIDN'T MATTER, SHE WOULDN'T NEED IT AFTERWARDS!! TALK ABOUT PROMISES. IT BREAKS MY HEART THAT THIS WAS EVER SAID.]

Tell patients that we are in the early stages of the understanding of this treatment.

[THIS IS ALL VERY PRACTICAL. SO FAR I LIKE DR. SULLIVAN.]

If possible, add to knowledge. Become part of a registry.

[VERY IMPORTANT! DO NOT LET THE DATA GO UNUSED.]

Be aware that there is a learning curve.

[I THINK THIS IS EXTREMELY SIGNIFICANT AS PATIENTS. A DOCTORS DOING HIS 1ST PATIENT IS NOT AS GOOD AT IT AS DOCTORS DOING THEIR 100TH PATIENT. LEARNING CURVE. THERE MIGHT BE LIFELONG CONSEQUENCES FOR THAT 1ST PATIENT THAT THE 100TH PATIENT DODGED. CHOOSE YOUR IR WISELY.]

Dr. Sullivan talks about the learning curve specific to CCSVI. How to diagnose. He encourages getting ultrasound or MR prior to procedure. Learn the symptoms of CCSVI, in order to assess if you've had a good result. Learn the angiographic findings, such as what and how to treat, in order to direct your therapy. Learn how to prevent or manage complications. Learn what to do for follow-up.

[THE ANGIOGRAPHIC FINDINGS, INCLUDING WHAT AND HOW TO TREAT, IS APPROACHED DIFFERENTLY BY DIFFERENT PROVIDERS, AND BY A PROVIDER IN THE EARLY STAGES OF BEGINNING TO TREAT CCSVI AND LATER ON WHEN HE HAS SEEN AND DONE MORE. LEARNING CURVE, DEFINITELY.]

This is an evolving field. Find a mentor if you can who is doing these in large volume. The internet can be a good source of information to both find out what the patients are thinking and also physicians are involved in some of these sites and you can learn from some very experienced physicians on these sites.

[LOOK AT THAT! HE LISTS THE TiMS WEBSITE AND CCSVI LOCATOR.]

You'll be asked how to integrate ccsvi treatment into ongoing therapy. You'll decide how to interact with neurologists. I tell patients it's up to them. Most patients say they are not going to tell their neurologists, that their neurologists are opposed, and that they will tell their neurologists after they have it done. Patients are on disease-modifying drug or alternative therapies.

Coding and billing: up until recently insurance uniformly paying. Just recently BCBS has stated that CCSVI is not medically necessary to be treated. What's important is the state the patient lives in, not the state you're practicing in.

[I THOUGHT IT WAS BOTH. HE ALSO LISTS BCBS MN AS ONE OF THE STATES WITH POLICIES AGAINST CCSVI BUT AS FAR AS I AM AWARE MN IS STILL GOOD. I WILL CHECK ON THAT.]

You'll have to decide on what to do about rejections. Appeal? Give the patients the code and have them do the appeal or have the office appeal? Determine cash charge for patients without insurance.

He lists the specific billing codes, if anyone is interested in those, for things like transluminal balloon angioplasty, placement of a stent, etc. None of the codes are specific to CCSVI.

Building a practice: you won't get referrals from neurologists. [lol!! Although he says he does get some but not many.] You can get involved in the online sites. [!] You can establish a diagnostic component to your practice. Direct patient marketing is also an option.

[WHILE DIRECT PATIENT MARKETING IS BEING DONE, SUCH AS ADVERTISEMENTS THAT STARTED POPPING UP ON FACEBOOK, IT IS QUESTIONABLE TO ME THAT THIS IS A PROCEDURE I WANT MARKETED TO PATIENTS AT THIS EARLY STAGE IN THE DISCOVERY.]

Patient evaluation involves reviewing the doppler, do a careful review of signs and symptoms, obtain history, answer questions, discuss treatment options.

You'll need to determine if you'll treat patients with CCSVI without MS. Determine if you're prepared to treat children. Can you handle complications and problems if you treat children in an outpatient ambulatory setting, without the back-up specialists at a hospital?

[SHOULD PATIENTS WITH CCSVI WITHOUT MS BE TREATED? SHOULD CHILDREN BE TREATED?]

Procedure: schedule as 2.5 hours when you start. Full anticoagulation during procedure, supine for four hours, no problems with hematomas. Nursing staff for recovery. Minimal post-procedure pain in these patients. Equipment: you need to be prepared for taller patients, which means exchange length guidewires, balloons on 120 cm shafts, and 90 cm diagnostic catheters. You can get by on smaller ones but don't want to be caught offguard when the longer ones are needed.

Followup: Distance, difficulty of travel for these patients may limit follow-up. He does telephone follow-up and email and visits based on symptoms. Email is an excellent means for procedure-based practice to provide detailed communication between MD and patient. He adds the email exchange to the patients' charts. To my patients if you view this online [OR READ CECE'S NOTES], if you haven't sent me an email, please do. It's really how we learn.
In an ideal world, he would get routine follow-up with ultrasound but doesn't know exactly what intervals it should be. With patients coming from a distance, it is difficult to have centers that can do these properly.

Mail order pharmacy can ship lovenox to patients' home.

Conclusions: you probably have the necessary skills if you're performing endovascular procedures but need to learn details related to CCSVI. You need to be comfortable with CCSVI controversy and some of the political or insurance barriers.

[MY CONCLUSION: WHILE IT IT BENEFICIAL TO PATIENTS TO HAVE LOCAL IR'S GETTING INTO CCSVI TREATMENT, THERE IS MUCH TO BE SAID FOR GOING WITH THE EXPERT OPTION, NOT THE LOCAL OPTION, WHEN THE EXPERT HAS GREATER EXPERIENCE. ANY IR'S INSPIRED BY THIS TALK TO GET INTO CCVSI WILL HAVE TO START UP THAT LEARNING CURVE. IN THE BEGINNING THEY DO NOT EVEN KNOW WHAT THEY DO NOT KNOW AND IT IS THE PATIENT THAT INCURS ANY DAMAGE THAT MIGHT HAVE BEEN PREVENTABLE WITH EXPERIENCE. I CANNOT REMEMBER WHICH IR IT WAS, BUT IT HAS BEEN SAID THAT CCSVI WAS THE MOST DIFFICULT LESIONS THEY HAD TREATED. IT IS A COMPLEX DISEASE THAT PRESENTS IN VARIABLE WAYS, IT IS NOT ALWAYS VALVES, ALTHOUGH IT IS OFTEN VALVES. THE JUGULARS ARE MORE FRAGILE THAN INITIALLY THOUGHT, WHEN THE OVERSIZED BALLOONS WERE BEING USED. AND IVUS WAS NOT MENTIONED AT ALL IN DR. SULLIVAN'S TALK. HE IS NOT EVEN SUGGESTING THAT NEWBIE IR'S PURCHASE AN IVUS BEFORE STARTING TO TREAT CCSVI, DESPITE THE UNDISPUTED VALUE OF IVUS IN INTERROGATING INTRALUMINAL ABNORMALITIES.]

[GREAT PRESENTATION BY DR. SULLIVAN. IF YOU'RE HIS PATIENT, SEND HIM AN EMAIL, LET HIM KNOW HOW YOU'RE DOING, OK?]
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